Protective effects of thymoquinone against acrylamide-induced liver, kidney and brain oxidative damage in rats

Acrylamide (AA), an industrial monomer, may cause multi-organ toxicity through induction of oxidative stress and inflammation. The antioxidant properties of thymoquinone (TQ), an active constituent of Nigella sativa , have been established before. The aim of the current study was to assess the prote...

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Bibliographic Details
Published in:Environmental science and pollution research international 2020-10, Vol.27 (30), p.37709-37717
Main Authors: Abdel-Daim, Mohamed M., Abo El-Ela, Fatma I., Alshahrani, Fatima K., Bin-Jumah, May, Al-Zharani, Mohammed, Almutairi, Bader, Alyousif, Mohamed S., Bungau, Simona, Aleya, Lotfi, Alkahtani, Saad
Format: Article
Language:English
Subjects:
Acrylamide
Alanine
Alkaline phosphatase
Antioxidants
Aquatic Pollution
Atmospheric Protection/Air Quality Control/Air Pollution
Biomarkers
Brain
Brain damage
Brain injury
Catalase
Creatinine
Cytokines
Deoxyguanosine
DNA damage
Earth and Environmental Science
Ecotoxicology
Environment
Environmental Chemistry
Environmental Health
Environmental science
Environmental Sciences
Glutathione
Glutathione peroxidase
Inflammation
Interleukin 6
Interleukins
Intoxication
Kidneys
Lipid peroxidation
Lipids
Liver
Nitric oxide
Oxidation
Oxidative stress
Peroxidase
Peroxidation
Renal function
Research Article
Serum levels
Superoxide dismutase
Supplements
Toxicity
Tumor necrosis factor-α
Urea
Waste Water Technology
Water Management
Water Pollution Control
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Summary:Acrylamide (AA), an industrial monomer, may cause multi-organ toxicity through induction of oxidative stress and inflammation. The antioxidant properties of thymoquinone (TQ), an active constituent of Nigella sativa , have been established before. The aim of the current study was to assess the protective effects of TQ against AA-induced toxicity in rats. Forty-eight male Wistar rats were divided into six groups each of eight rats. The first group acted as a negative control and received normal saline. Groups II and III were administered TQ orally at doses of 10 and 20 mg/kg b.wt., respectively, for 21 days. The four group received AA (20 mg/kg b.wt.) for 14 days. The five and six groups were given TQ at either dose for 21 days, starting seven days before AA supplementation (for 14 days). Acrylamide intoxication was associated with significant ( p < 0.05) increases in serum levels of liver injury biomarkers (alanine transferase, aspartate transferase, and alkaline phosphatase), renal function products (urea, creatinine), DNA oxidative damage biomarker (8-oxo-2′-deoxyguanosine), and pro-inflammatory biomarkers (interleukin-1β, interleukin-6, and tumor necrosis factor-α). Moreover, AA intoxication was associated with increased lipid peroxidation and nitric oxide levels, while reduced glutathione concentration and activities of glutathione peroxidase, superoxide dismutase, and catalase in the liver, kidney, and brain. TQ administration normalized AA-induced changes in most serum parameters and enhanced the antioxidant capacity in the liver, kidney, and brain tissues in a dose-dependent manner. In conclusion, the current experiment showed that TQ exerted protective and antioxidant activities against AA-induced toxicity in mice.
ISSN:0944-1344
1614-7499
DOI:10.1007/s11356-020-09516-3